Shock

1. Shock Eric Anderson, DO Intern Survival Series Emergency Medicine Program Metro Health Hospital August 1, 2007

2. Definition Circulatory insufficiency that creates an imbalance between tissue oxygen supply and demand

3. Basics of Oxygen Supply and Circulation 1. Systemic O2 delivery = Cardiac output (CO) x Arterial O2 content 2. CO = Stroke Volume (SV) x Heart Rate (HR) 3. Mean Arterial Pressure (MAP) = CO x Systemic Vascular Resistance (SVR)

4. Autonomic Response Actions taken to maintain perfusion to essential organs 1. Arteriolar vasoconstriction: shunt blood from periphery 2. Increase HR and contractility to increase CO 3. Constriction of venous capacitance to increase venous return 4. Release of hormones (epi, norepi, dopamine, cortisol, etc.) to increase arterial and venous tone to increase MAP 5. Stimulation of the Renin-angiotensin system

5. Cellular Effects of Shock 1. ATP depletion causing ion-pump dysfunction: Na+ in, K+ out, cellular edema 2. Lysosomal enzymes released causing damage 3. Cellular death causing hemoconcentration, hyperkalemia, hyponatremia, alterations in glucose levels, lactic acidosis, pre-renal azotemia

6. Overall Response to Shock 1. SIRS: >/= 2 a) Alteration in temperature: <98.6 or >100.4 b) Tachycardia > 100 bpm c) Tachypnea > 20 bpm d) WBC < 4 or >12 or bandemia

7. Later� 2. MODS: Multisystem organ dysfunction caused by an imbalance of chemical mediators a) Myocardial depression b) Adult Respiratory Distress Syndrome (ARDS) c) DIC d) Hepatic failure e) Renal failure

8. Fluid and Blood Resuscitation Initial therapy for disorders causing intravascular volume depletion and resulting in tissue underperfusion and damage 1. Fluid spaces: a) Total Body Water (TBW) is 60% of adult bodyweight (42 L in 70 kg person) b) Intracellular is 2/3 of TBW (28 L in 70 kg person) c) Extracellular is 1/3 of TBW (14 L in 70 kg person) d) Intravascular is about 12% of TBW or 5-5.5 L

9. Isotonic Fluid Infusion Rates 18 G peripheral IV: 50-60 ml/min (under pressure can increase to 120-180 ml/min) 14 G PIV: 125-160 ml/min Central line venous introducer: 200 ml/min up to 400-500 ml/min under pressure

10. Resuscitation Fluids 1. Isotonic crystalloid: 0.9% NS or LR 2. Colloids: 5% or 25% Albumin, FFP 3. Hypertonic Solutions: 3 or 7.5% Saline 4. PRBC�s 5. Whole blood

11. Isotonic crystalloid: NS or LR leaks out of vasculature due to lack of large molecules to keep fluid in � therefore a 3:1volume must be infused Blood transfusion: Don�t use whole blood anymore; consider giving blood to hypotensive patient after 2-3 L of crystalloid - Type/crossmatch preferable, followed by type specific, followed by O- in order of preference - Large transfusions may require Platelets and FFP to avoid coagulopathy

12. Colloid Resuscitation: generally only used in hemorrhagic shock; good theory � give large molecules to hold fluids in the intravascular space; unfortunately does not work very well

13. Hypertonic Fluid Resuscitation: To draw fluids from interstitial space to maintain intravascular volume; may be specifically helpful in head injury patients to decrease ICP; has not been shown to improve outcome compared to isotonic fluids

14. Oxygen-carrying Fluids: Experimental hemoglobin or fluorocarbon-based oxygen carrying fluids due alleviate the fact that crystalloid may increase intravascular volume and therefore support pressure but it does not transport oxygen

15. Assessing response to resuscitation: probably best done with invasive monitoring of central venous pressure; ABG, urine output, lactic acid levels and other parameters can be helpful and are often used as well in the ICU

16. Septic Shock Caused by any micro-organism though gram-negative is more common than gram-positive Epidemiology of Sepsis: 3 cases per 1000 people, 2.26 per 100 admitted patients, up to half develop septic shock with a mortality of 45%

17. Definitions: 1. SIRS: systemic inflammatory response to a variety of severe clinical insults 2. Sepsis: SIRS with a septic source 3. Severe sepsis: Sepsis associated with end-organ dysfunction 4. Septic shock: Sepsis induced hypotension despite adequate fluid resuscitation usually requires pressor support

18. Pathophysiology: Locus of infection enters the bloodstream releasing toxins or components causing a cascade of humoral defense mechanisms that alter cardiac, peripheral resistance, and permeability causing effects seen in patients

19. Clinical features: 1. Constitutional: hypo- or hyperthermia, tachycardia, widened pulse-pressure, tachypnea, mental status changes 2. Cardiovascular: Early: warm shock due to increased CO and peripheral dilation/Late: cold shock due to myocardial depression then decreased perfusion

20. Pulmonary: Most common condition associated with ARDS Renal: decreased perfusion can result in renal failure Hepatic: �Shock liver� due to decreased perfusion or hepatocellular dysfunction Hematologic: Blood loss, thrombocytopenia, DIC

21. Endocrine: Hyper- and hypoglycemia Acid/base: Early respiratory alkalosis then later becoming metabolic acidosis as perfusion is further compromised

22. Diagnosis: Any patient with temp <36 or> 38, a systolic BP < 90 especially if patient does not respond to 1 L IV crystalloid. Consider other causes of shock. Most common cause of septic shock in adults with CNS infection is gram negative meningitis; pulmonary is bacterial pneumonia; others

23. Studies: CBC, DIC panel, electrolytes, LFT, ABG, U/A, blood cultures, CRP, lactic acid, etc.

24. Treatment: 1. A: Airway 2. B: Breathing 3. C: Circulation: Hemodynamic stabilization: IVF, inotropic support 4. Hemodynamic endpoints: maintain CVP, UO, respiratory status 5. Empiric antibiotics 6. Remove source of infection

25. Cardiogenic Shock Defined as a state of diminished CO producing inadequate perfusion despite adequate circulating volume Etiology: Usually due to AMI that effects > 40% of the LV with an overall mortality rate of 60-90%; incidence of cardiogenic shock in patients with AMI is 6-8% with a mean time of onset 8 hours after AMI

26. Pathophysiology: Most often from AMI; acute CHF occurs with loss of >25% of LV/ shock ensues with > 40% loss Other causes can include ventricular wall rupture, acute mitral regurgitation, aortic stenosis, acute aortic regurgitation

27. Occult cardiogenic shock in patients with CHF may be difficult to identify To compensate for loss of SV, tachycardia develops which decreases SV and coronary blood flow further; increased sympathetic tone and activation of the renin-angiotensin system worsens the situation by increasing the workload of the heart

28. RV infarction can further worsen the situation in inferior AMI by causing hypotension � posterior AMI must maintain adequate volume to ensure preload as RV SV depends on fluid volume almost exclusively

29. History/Physical Examination: May be difficult depending on presentation; usually involves SOB or chest discomfort; hypotension is common but may not be <90 if chronic hypertension is present; Pulse pressure may be widened; Signs of CHF may be present

30. Ancillary studies: EKG CXR BNP Cardiac enzymes Echocardiography Hemodynamic monitoring

31. Treatment: ABC�s Stabilization of rhythm, electrolyte abnormalities, volume status ASAP AMI: aspirin, Integrilin, Heparin/Lovenox, NTG, ACEI, b-blockers Hypotension: If no sign of CHF is present, use a small IVF bolus; Inotropes should be used carefully as they can support pressure but they do increase myocardial oxygen demand at a time supply is already compromised

32. Pure peripheral vasoconstrictors are generally contraindicated If acute regurgitation is suspected/diagnosed, may use a combination of dobutamine (increase contractility) and nitroprusside (decrease TPR)

33. Reperfusion: Early revascularization is the key Cardiac cath lab: AMI patients with ST segment elevation go NOW Thrombolytics: lowest mortality rate was actually found in patients where thrombolytics were followed quickly by revascularization Intra-aortic balloon pumps can be used

34. Anaphylactic Shock Severe hypersensitivity reaction characterized by multisystem involvement which may compromise both airway and induce hypotension resulting from a massive release of chemical mediators from mast cells and basophils in an IgE dependent manner. Anaphylactoid reactions can also occur in a non-IgE dependent manner.

35. Epidemiology: Age, race, occupation, gender and geography cannot predict anaphylaxis. Atopic patients are at no more risk than non-atopic patients. Poorly controlled asthma and previous anaphylactic reactions are risk factors for fatal anaphylaxis. Rates in the ED are 0.02 � 0.5% of overall patients.

36. Pathophysiology: Mast cell and basophil degranulation and mediator release cause IgE cross-linking complement activation, modulation of arachidonic acid pathways. Classic pathway is having a second exposure trigger an inappropriate response in the sensitized patient.

37. Clinical features often include respiratory and/or cardiovascular compromise, and typically involve urticaria and angioedema. Other symptoms can be rhinorrhea, V/D, abdominal pain, nausea, dysrhythmia. Vast majority of symptoms occur within 1 hour of exposure. Generally, the faster the onset of symptoms, the worse the reaction will be.

38. Diagnosis is made clinically and there are no ancillary tests to help. Serum tryptase levels can confirm later.

39. Treatment: Emergent: Epi 3 cc of 1:1000 SQ, ABC�s, IVF First line agents: 1. Epi SQ or IM 2. Epi IV: 0.1 mg in 1:100,000 dilution over 5-10minutes; if refractory, give 1 mg in 500 cc D5W running at 0.5-2 cc/min

40. Second-line agents: Corticosteroids: Methylprednisolone or hydrocortisone Anti-histamines: H1 (benadryl), H2 (Pepcid) Anti-bronchospastics: Albuterol, magnesium Glucagon for those on b-blockers may be required

41. Neurogenic Shock Characterized by hypotension and bradcardia occurring after spinal cord injury that disrupts sympathetic tone to vital organs leaving unopposed vagal tone Must differentiate from spinal shock that involves transient loss of reflexes below level of insult

42. Epidemiology: Usually blunt trauma � only 10% of spinal cord injuries are due to penetrating trauma; most in US involve MVC with cervical region being most common followed by (in order of frequency): thoracolumbar > thoracic > lumbar

43. Pathophysiology: Sympathetic tone is maintained through responses from sympathetic neuronal cell bodies in the region of T1-L2. Injury above or in this area will decrease sympathetic tone to organs innervated leaving them stimulated by vagal (parasympathetic) tone only. Primary injury is at time of trauma. Secondary injury is visible on MRI later and is due to ischemia to cord caused by inciting event.

44. Clinical features: Hypotension, bradycardia, widened pulse pressure, warm/dry skin, possible hypothermia. Symptoms may last for up to 3 weeks. The higher the injury, the worse the presentation.

45. Treatment: 1. ABC�s 2. D: Disability or neurologic evaluation performed during trauma evaluation Hypotension treated with IVF to keep MAP 85-90 Severe bradycardia treated with Atropine Consult Neurosurgery quickly Steroids have questionable benefit (at best) � use methylprednisolone 30 mg/kg IV bolus then 5.4 mg/kg/hr over the next 23 hours